An angiotensin-II analogue with a sulfated tyrosine residue was prepared by arylsulfotransferase treatment of synthetic human angiotensin-II. Its biological activities were studied in isolated smooth muscles, and its effect on blood pressure was determined. The sulfated angiotensin-II (AII-S) was about 15-30 fold less potent than angiotensin-II (AII) for ileum contraction and gallbladder contraction. The hypertensive potency of AII-S was about 30-fold less than that of AII.

The pharmacological activities of synthetic human CCK-33, in which a tyrosine molecule was sulfated by arylsulfotransferase, were investigated in the rat and the guinea-pig. The activities were compared with those of non-sulfated CCK-33 (CCK-33NS), CCK-8 and CCK-4. CCK-33 was about 100 fold more potent than non-sulfated CCK-33(CCK-33NS) but was about 20 fold less potent than CCK-8 in the contraction of the isolated gallbladder of the guinea-pig. In rat pancreatic secretion, intravenous CCK-33 and CCK-8 showed almost the same activity. The potency of each was about 1000 fold more than the individual potency of CCK-33NS, non-sulfated CCK-8 (CCK-8NS) and CCK4. There were no significant differences in gastric acid stimulatory activities among CCK-33, CCK-8, CCK-4, but the activities of CCK-33NS and CCK-8NS were less than those of CCK-33 and CCK-8, respectively. CCK-33 and CCK-8 produced a reduction in the intake of powder chow in doses of 10(-8) and 3 x 10(-8) mol/kg i.p., but CCK-33NS, CCK-8NS and CCK-4 did not. In conclusion, the activities of synthetic human CCK-33 are almost the same as those of CCK-8 on exocrine pancreatic secretion, gastric acid secretion and food intake, but less than CCK-8 on isolated gallbladder contraction.

We have studied the fibrinolytic effect of VIP in rats. Intravenous injection of VIP enhanced blood fibrinolytic activity in a dose-related manner. The euglobulin fraction obtained from intact rat plasma incubated with VIP did not produce an increase in fibrinolytic activity, while dextran sulfate (DS) and urokinase (UK) showed the activity. VIP solution placed on a plasminogen-rich fibrin plate did not show fibrinolysis. VIP had neither a plasminogen activator nor plasmin activity. VIP may release plasminogen activators into the blood.